Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Genetic and Molecular Bases of the Circadian Rhythms

Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 January 2019) | Viewed by 32055

Share This Special Issue

Special Issue Editor

Prof. Dr. Ralf Stanewsky

E-Mail Website
Guest Editor

Institute of Neuro- and Behavioral Biology, Westfälische Wilhelms University, Münster, Germany
Interests: circadian clocks; synchronization of circadian clocks to environmental light and temperature cycles; Drosophila neurogenetics; photoreceptors; thermoreceptors; sensory integration; sleep/wake rhythms; bioluminescence reporter genes; period; timeless; cryptochrome

Special Issue Information

Dear Colleagues,

In 2017, the Nobel Prize for Physiology or Medicine was awarded to Jeffrey C. Hall, Michael Rosbash, and Michael W. Young for their discoveries of molecular mechanisms that control circadian rhythms. Their findings were largely based on forward genetic approaches in the fruit fly, Drosophila melanogaster, and provided a comprehensive picture of how transcriptional and translational molecular feedback loops regulate the rhythmic expression of clock genes, clock controlled genes, and behavior. In recent years, the focus of Drosophila clock researchers has shifted towards understanding the specific roles of the various clock neurons in the fly brain, how they are coupled to each other, and how they are synchronized to environmental cycles of light and temperature. Still forward genetic and modern neurogenetic tools (e.g., optogenetics and genetically encoded calcium sensors) play a major role in understanding the function and architecture of the neuronal network controlling circadian rhythms in the fly. The current Special Issue gives an opportunity to either review recent work in this area or to contribute original findings, or both. Where possible (and if you wish, in honor to our three Nobel Laureates), emphasis should be put on how classical and modern genetic approaches contributed to our current understanding of the Drosophila circadian clock.

Prof. Dr. Ralf Stanewsky
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

circadian clock
neurogenetics
neuronal circuits
calcium imaging
optogenetics
period
timeless
cryptochrome
clock
cycle

Published Papers (5 papers)

Download All Papers

Research

Jump to: Review

12 pages, 1751 KiB

Open AccessArticle

The Circadian tau Mutation in Casein Kinase 1 Is Part of a Larger Domain That Can Be Mutated to Shorten Circadian Period

by Anandakrishnan Venkatesan, Jin-Yuan Fan, Samuel Bouyain and Jeffrey L. Price

Int. J. Mol. Sci. 2019, 20(4), 813; https://doi.org/10.3390/ijms20040813 - 14 Feb 2019

Cited by 7 | Viewed by 2672

Abstract

Drosophila Double-time (DBT) phosphorylates the circadian protein Period (PER). The period-altering mutation tau, identified in hamster casein kinase I (CKIε) and created in Drosophila DBT, has been shown to shorten the circadian period in flies, as it does in hamsters. Since CKI often phosphorylates downstream of previously phosphorylated residues and the tau amino acid binds a negatively charged ion in X-ray crystal structures, this amino acid has been suggested to contribute to a phosphate recognition site for the substrate. Alternatively, the tau amino acid may affect a nuclear localization signal (NLS) with which it interacts. We mutated the residues that were close to or part of the phosphate recognition site or NLS. Flies expressing DBT with mutations of amino acids close to or part of either of these motifs produced a shortening of period, suggesting that a domain, including the phosphate recognition site or the NLS, can be mutated to produce the short period phenotype. Mutation of residues affecting internally placed residues produced a longer period, suggesting that a specific domain on the surface of the kinase might generate an interaction with a substrate or regulator, with short periods produced when the interaction is disrupted. Full article

(This article belongs to the Special Issue Genetic and Molecular Bases of the Circadian Rhythms)

► Show Figures

Figure 1

Review

Jump to: Research

15 pages, 1184 KiB

Open AccessReview

Smith-Magenis Syndrome: Molecular Basis of a Genetic-Driven Melatonin Circadian Secretion Disorder

by Alice Poisson, Alain Nicolas, Idriss Bousquet, Véronique Raverot, Claude Gronfier and Caroline Demily

Int. J. Mol. Sci. 2019, 20(14), 3533; https://doi.org/10.3390/ijms20143533 - 19 Jul 2019

Cited by 8 | Viewed by 4271

Abstract

Smith-Magenis syndrome (SMS), linked to Retinoic Acid Induced (RAI1) haploinsufficiency, is a unique model of the inversion of circadian melatonin secretion. In this regard, this model is a formidable approach to better understand circadian melatonin secretion cycle disorders and the role of the RAI1 gene in this cycle. Sleep-wake cycle disorders in SMS include sleep maintenance disorders with a phase advance and intense sleepiness around noon. These disorders have been linked to a general disturbance of sleep-wake rhythm and coexist with inverted secretion of melatonin. The exact mechanism underlying the inversion of circadian melatonin secretion in SMS has rarely been discussed. We suggest three hypotheses that could account for the inversion of circadian melatonin secretion and discuss them. First, inversion of the circadian melatonin secretion rhythm could be linked to alterations in light signal transduction. Second, this inversion could imply global misalignment of the circadian system. Third, the inversion is not linked to a global circadian clock shift but rather to a specific impairment in the melatonin secretion pathway between the suprachiasmatic nuclei (SCN) and pinealocytes. The development of diurnal SMS animal models that produce melatonin appears to be an indispensable step to further understand the molecular basis of the circadian melatonin secretion rhythm. Full article

(This article belongs to the Special Issue Genetic and Molecular Bases of the Circadian Rhythms)

► Show Figures

Figure 1

13 pages, 2172 KiB

Open AccessReview

Drosophila Temperature Preference Rhythms: An Innovative Model to Understand Body Temperature Rhythms

by Tadahiro Goda and Fumika N. Hamada

Int. J. Mol. Sci. 2019, 20(8), 1988; https://doi.org/10.3390/ijms20081988 - 23 Apr 2019

Cited by 14 | Viewed by 4822

Abstract

Human body temperature increases during wakefulness and decreases during sleep. The body temperature rhythm (BTR) is a robust output of the circadian clock and is fundamental for maintaining homeostasis, such as generating metabolic energy and sleep, as well as entraining peripheral clocks in mammals. However, the mechanisms that regulate BTR are largely unknown. Drosophila are ectotherms, and their body temperatures are close to ambient temperature; therefore, flies select a preferred environmental temperature to set their body temperature. We identified a novel circadian output, the temperature preference rhythm (TPR), in which the preferred temperature in flies increases during the day and decreases at night. TPR, thereby, produces a daily BTR. We found that fly TPR shares many features with mammalian BTR. We demonstrated that diuretic hormone 31 receptor (DH31R) mediates Drosophila TPR and that the closest mouse homolog of DH31R, calcitonin receptor (Calcr), is essential for mice BTR. Importantly, both TPR and BTR are regulated in a distinct manner from locomotor activity rhythms, and neither DH31R nor Calcr regulates locomotor activity rhythms. Our findings suggest that DH31R/Calcr is an ancient and specific mediator of BTR. Thus, understanding fly TPR will provide fundamental insights into the molecular and neural mechanisms that control BTR in mammals. Full article

(This article belongs to the Special Issue Genetic and Molecular Bases of the Circadian Rhythms)

► Show Figures

Graphical abstract

25 pages, 988 KiB

Open AccessReview

Off the Clock: From Circadian Disruption to Metabolic Disease

by Eleonore Maury

Int. J. Mol. Sci. 2019, 20(7), 1597; https://doi.org/10.3390/ijms20071597 - 30 Mar 2019

Cited by 86 | Viewed by 11469

Abstract

Circadian timekeeping allows appropriate temporal regulation of an organism’s internal metabolism to anticipate and respond to recurrent daily changes in the environment. Evidence from animal genetic models and from humans under circadian misalignment (such as shift work or jet lag) shows that disruption of circadian rhythms contributes to the development of obesity and metabolic disease. Inappropriate timing of food intake and high-fat feeding also lead to disruptions of the temporal coordination of metabolism and physiology and subsequently promote its pathogenesis. This review illustrates the impact of genetically or environmentally induced molecular clock disruption (at the level of the brain and peripheral tissues) and the interplay between the circadian system and metabolic processes. Here, we discuss some mechanisms responsible for diet-induced circadian desynchrony and consider the impact of nutritional cues in inter-organ communication, with a particular focus on the communication between peripheral organs and brain. Finally, we discuss the relay of environmental information by signal-dependent transcription factors to adjust the timing of gene oscillations. Collectively, a better knowledge of the mechanisms by which the circadian clock function can be compromised will lead to novel preventive and therapeutic strategies for obesity and other metabolic disorders arising from circadian desynchrony. Full article

(This article belongs to the Special Issue Genetic and Molecular Bases of the Circadian Rhythms)

► Show Figures

Figure 1

22 pages, 1156 KiB

Open AccessReview

Circadian Rhythm Abnormalities in Parkinson’s Disease from Humans to Flies and Back

by Federica De Lazzari, Marco Bisaglia, Mauro Agostino Zordan and Federica Sandrelli

Int. J. Mol. Sci. 2018, 19(12), 3911; https://doi.org/10.3390/ijms19123911 - 06 Dec 2018

Cited by 34 | Viewed by 8412

Abstract

Clinical and research studies have suggested a link between Parkinson’s disease (PD) and alterations in the circadian clock. Drosophila melanogaster may represent a useful model to study the relationship between the circadian clock and PD. Apart from the conservation of many genes, cellular mechanisms, signaling pathways, and neuronal processes, Drosophila shows an organized central nervous system and well-characterized complex behavioral phenotypes. In fact, Drosophila has been successfully used in the dissection of the circadian system and as a model for neurodegenerative disorders, including PD. Here, we describe the fly circadian and dopaminergic systems and report recent studies which indicate the presence of circadian abnormalities in some fly PD genetic models. We discuss the use of Drosophila to investigate whether, in adults, the disruption of the circadian system might be causative of brain neurodegeneration. We also consider approaches using Drosophila, which might provide new information on the link between PD and the circadian clock. As a corollary, since PD develops its symptomatology over a large part of the organism’s lifespan and given the relatively short lifespan of fruit flies, we suggest that genetic models of PD could be used to perform lifelong screens for drug-modulators of general and/or circadian-related PD traits. Full article

(This article belongs to the Special Issue Genetic and Molecular Bases of the Circadian Rhythms)

► Show Figures